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. Author manuscript; available in PMC: 2019 Apr 26.
Published in final edited form as: Cancer Res. 2018 Mar 27;78(11):2939–2951. doi: 10.1158/0008-5472.CAN-17-1944

Figure 4. IKKα deletion ameliorates respiratory epithelial oncogenicity of mutant KRASG12D.

Figure 4

Conditional IKKα (Chukf/f) or IKKβ (Ikbkbf/f) gene-deleted mice were intercrossed with mice carrying a loxP-STOP-loxP.KRASG12D conditional allele (LSL.KRASG12D; all C57BL/6) and their offspring received 5 x 108 PFU intratracheal Ad- Cre and was killed four months later. (A) Schematic of experimental time-course (boxes= months) and topology of IKK-deleted (pink cytosol) versus KRASG12D-mutant (red nucleus) cells in this model, where IKK-deletion and oncogenic KRASG12D expression uniquely coincide in the same cells. (B) Frequency distribution of lung tumorigenesis with n and χ2 P values. ns, *, **, and ***: P > 0.05, P < 0.05, P < 0.01, and P < 0.001, respectively, for the indicated comparisons by Fischer’s exact test. (C, D) Data summary of relative lung tumor fraction and total lung tumor volume (burden) per lung with raw data points (dots), Tukey’s whiskers (boxes: interquartile range; bars: 50% extreme quartiles), and Kruskal-Wallis ANOVA P values. ns, *, **, and ***: P > 0.05, P < 0.05, P < 0.01, and P < 0.001, respectively, for the indicated comparisons by Dunn’s post-tests. (E) Representative hematoxylin and eosin-stained lung tissue sections. Arrows denote lung tumors.